Jasmonate (JA) and ethylene (ET) are two major plant hormones that synergistically regulate plant development and tolerance to necrotrophic fungi. Both JA and ET induce the expression of several pathogenesis-related genes, while blocking either signaling pathway abolishes the induction of these genes by JA and ET alone or in combination. However, the molecular basis of JA/ET coaction and signaling interdependency is largely unknown. Here, we report that two Arabidopsis ET-stabilized transcription factors (EIN3 and EIL1) integrate ET and JA signaling in the regulation of gene expression, root development, and necrotrophic pathogen defense. Further studies reveal that JA enhances the transcriptional activity of EIN3/EIL1 by removal of JA-Zim domain (JAZ) proteins, which physically interact with and repress EIN3/EIL1. In addition, we find that JAZ proteins recruit an RPD3-type histone deacetylase (HDA6) as a corepressor that modulates histone acetylation, represses EIN3/EIL1-dependent transcription, and inhibits JA signaling. Our studies identify EIN3/EIL1 as a key integration node whose activation requires both JA and ET signaling, and illustrate transcriptional derepression as a common mechanism to integrate diverse signaling pathways in the regulation of plant development and defense.root hair | Botrytis cinerea P lants are sessile organisms and face different environmental changes during their lifespan. To survive various abiotic and biotic stresses, plants synthesize a number of small molecules functioning as phytohormones to elaborately regulate their growth, development, and defense. Two types of phytohormonesethylene (ET) and jasmonate (JA)-are crucial for plant development and defense against necrotrophic fungi infections (1-3). Complicated modes of interaction between ET and JA have been documented in different processes. For example, ET strongly suppresses JA-induced wounding-responsive gene expression, but JA suppresses ET-induced apical hook formation (4, 5), indicative of their antagonisms. Upon necrotrophic fungi infections, plants can quickly produce ET and JA and induce the expression of downstream defense genes (like ERF1, ORA59, and PDF1.2) that help plants tolerate or fight against the fungal pathogens (1). Plants treated with exogenous JA or ET express high levels of defense genes (6, 7), and simultaneous treatment with JA and ET results in the highest expression (8). Nevertheless, in the ET or JA insensitive mutant (ein2 or coi1, respectively), JA and ET alone or in combination fail to induce the expression of those defense genes (8, 9), indicating that the two hormone-signaling pathways are required concomitantly for the activation of plant-defense response. These results suggest that JA and ET act synergistically and mutually dependently in regulating necrotrophic pathogen responses. However, the molecular details underlying such hormone synergy and signaling interdependency are currently unknown.ET is a gaseous hormone, which is perceived by its receptors and represses a Raf-like kinase CON...

The Arabidopsis root has a unique cellular pattern in its singlelayered epidermis. Cells residing over the intercellular spaces between underlying cortical cells (H position) differentiate into hair cells, whereas those directly over cortical cells (N position) differentiate into non-hair cells. Recent studies have revealed that this cellular pattern is determined by interactions of six patterning genes CPC, ETC, GL2, GL3͞EGL3, TTG, and WER, and that the position-dependent expression of the CPC, GL2, and WER genes is essential for their appropriate interactions. However, little is known about how the expressions of the pattern genes are determined. Here we show that trichostatin A (TSA) treatment of germinating Arabidopsis seedlings alters the cellular pattern of the root epidermis to induce hair cell development at nonhair positions. The effects of TSA treatment are rapid, reversible, concentration-dependent, and position-independent. TSA inhibition of histone deacetylase activity results in hyperacetylation of the core histones H3 and H4, and alters the expression levels and cell specific expression of the patterning genes CPC, GL2 and WER. Analysis of histone deacetylase mutant cellular patterning further verified the participation of histone acetylation in cellular patterning, and revealed that HDA18 is a key component in the regulatory machinery of the Arabidopsis root epidermis. We propose a working model to suggest that histone acetylation may function in mediating a positional cue to direct expression of the patterning genes in the root epidermal cells.histone as a signaling mediator ͉ trichostatin A ͉ histone deacetylase ͉ positional cue ͉ chromatin immunoprecipitation

K201 (JTV519), a benzothiazepine derivative, has been shown to possess anti-arrhythmic and cardioprotective properties, but the mechanism of its action is both complex and controversial. It is believed to stabilize the closed state of the RyR2 (cardiac ryanodine receptor) by increasing its affinity for the FKBP12.6 (12.6 kDa FK506 binding protein) [Wehrens, Lehnart, Reiken, Deng, Vest, Cervantes, Coromilas, Landry and Marks (2004) Science 304, 292-296]. In the present study, we investigated the effect of K201 on spontaneous Ca2+ release induced by Ca2+ overload in rat ventricular myocytes and in HEK-293 cells (human embryonic kidney cells) expressing RyR2 and the role of FKBP12.6 in the action of K201. We found that K201 abolished spontaneous Ca2+ release in cardiac myocytes in a concentration-dependent manner. Treating ventricular myocytes with FK506 to dissociate FKBP12.6 from RyR2 did not affect the suppression of spontaneous Ca2+ release by K201. Similarly, K201 was able to suppress spontaneous Ca2+ release in FK506-treated HEK-293 cells co-expressing RyR2 and FKBP12.6. Furthermore, K201 suppressed spontaneous Ca2+ release in HEK-293 cells expressing RyR2 alone and in cells co-expressing RyR2 and FKBP12.6 with the same potency. In addition, K201 inhibited [3H]ryanodine binding to RyR2-wt (wild-type) and an RyR2 mutant linked to ventricular tachycardia and sudden death, N4104K, in the absence of FKBP12.6. These observations demonstrate that FKBP12.6 is not involved in the inhibitory action of K201 on spontaneous Ca2+ release. Our results also suggest that suppression of spontaneous Ca2+ release and the activity of RyR2 contributes, at least in part, to the anti-arrhythmic properties of K201.

The differentiation of hair (H) and non-hair (N) cells in the Arabidopsis thaliana root epidermis is dependent on positional relationships with underlying cortical cells. We previously found that histone acetylation relays positional information and that a mutant altered in the histone deacetylase gene family member HISTONE DEACETYLASE 18 (HDA18) exhibits altered H and N epidermal cell patterning. Here, we report that HDA18 has in vitro histone deacetylase activity and that both mutation and overexpression of HDA18 led to cells at the N position having H fate. The HDA18 protein physically interacted with histones related to a specific group of kinase genes, which are demonstrated in this study to be components of a positional information relay system. Both down-and upregulation of HDA18 increased transcription of the targeted kinase genes. Interestingly, the acetylation levels of histone 3 lysine 9 (H3K9), histone 3 lysine 14 (H3K14) and histone 3 lysine 18 (H3K18) at the kinase genes were differentially affected by down-or upregulation of HDA18, which explains why the transcription levels of the four HDA18-target kinase genes increased in all lines with altered HDA18 expression. Our results reveal the surprisingly complex mechanism by which HDA18 affects cellular patterning in Arabidopsis root epidermis.